Nō to shinkei = Brain and nerve
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The authors studied intracranial hemodynamics in experimental animals (Macaca Fuscatus) with acute intracranial hypertension by use of transcranial Doppler (TCD) ultrasound. The blood mean flow velocity in the middle cerebral artery (MCA-FV) and pulsatility index (PI) was recorded using TCD ultrasound (TC2-64, EME) as in the clinical study. Acute intracranial hypertension was produced to determine the correlation of MCA-FV with intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in 11 monkeys, and the correlation of PI with ICP and CPP in 7 monkeys. ⋯ All PI values were above 1.0 when CPP was 40mmHg or less. Thus, we could not estimate the absolute values of ICP or CPP from MCA-FV and PI. It seems possible, however, to follow changes in intracranial hemodynamics at the time of increased ICP if MCA-FV and PI are measured continuously while paying attention to factors influencing MCA-FV.(ABSTRACT TRUNCATED AT 250 WORDS)
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Case Reports
[SPECT (single photon emission computed tomography) findings in 4 cases of neuronal migration disorders].
We report SPECT findings in four children with various types of neuronal migration disorders. SPECT of a patient with heterotopia showed a protrudent abnormal shadow into the centrum semiovale, the density of which was same as that of normal gray matter. The function and the metabolism of heterotopia appear same as those of the normal gray matter. ⋯ These pathologies may be related to our SPECT findings. SPECT of a patient with cortical dysplasia showed extensive lesions of decreased blood flow which was more wide spread than abnormal lesions detected by MRI. SPECT may be more sensitive than MRI to detect cortical dysplasias.
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In order to produce syringomyelia, localized arachnoiditis was created in adult New Zealand albino rabbits and Wistar rats by the injection of kaolin into the thoracic spinal subarachnoid space and incision of the dura mater of the thoracic spinal cord. The rabbits and rats were divided into 3 groups; the control group, dural incision group (DG) and kaolin injection group (KG). Each rabbit was sacrificed at 4, 8, 12 and 16 weeks after the operation. ⋯ In the cord parenchyma adjacent to the arachnoiditis, multiple spots of demyelination due secondary to ischemia demonstrated by LFB stain were noted. On the other hand, in the cord with the pia-arachnoid remained uninvolved, no demyelination was observed. (6) Localized adhesive arachnoiditis consisted of proliferation of fibrous tissue, lymphocytic infiltration and obliterating processes of small pial vessels involved in it. These data suggest that the cavitation within the cord would be induced by the ischemia, and hydromyelia would be produced by the pressure dissociation between the spinal subarachnoid space and the central canal.
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The cause of hyponatremia following subarachnoid hemorrhage (SAH) has been understood as an inappropriate secretion of antidiuretic hormone (SIADH). Whereas, water restriction for the management of this condition sometimes induces a severe dehydration, resulting in vasospasm. To clarify the pathogenesis of hyponatremia following SAH, we measured the daily sodium and water balance with the plasma concentration of atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), and plasma renin activity (PRA) in seventeen cases after subarachnoid hemorrhage. ⋯ These correlations suggested that hyponatremia after SAH is the result of natriuresis by an increased ANP rather than ADH. In conclusion, a greater replenishment of water and sodium is required to avoid hyponatremia with dehydration. This technique may be helpful for the prevention of vasospasms following SAH.
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We studied retrospectively the relationship between hyponatremia and cerebral vasospasm in 121 consecutive patients with aneurysmal subarachnoid hemorrhage. In 19 patients sodium levels fell below 130 mEq/l on at least two consecutive days. Hyponatremia developed at average 8.9 hospital day and lasted for 4.4 days. ⋯ So, it is difficult to predict the development of vasospasm from that of hyponatremia. This study found incidence of cerebral vasospasm after aneurysmal subarachnoid hemorrhage to be significantly higher in patients who developed hyponatremia, which raised suspicion about the presence of dehydration. Hyponatremia with central origin generally remains asymptomatic, but it is important to treat positively when the pathology of cerebral vasospasm is taken into consideration.